Open AccessCigarette smoke extract-induced p120-mediated NF-κB activation in human epithelial cells is dependent on the RhoA/ROCK pathway
Author(s) -
Chao Zhang,
Shenghui Qin,
Lingzhi Qin,
Liwei Liu,
Wenjia Sun,
Xiyu Li,
Naping Li,
Renliang Wu,
Xi Wang
Publication year - 2016
Publication title -
scientific reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.24
H-Index - 213
ISSN - 2045-2322
DOI - 10.1038/srep23131
Subject(s) - rhoa , adherens junction , inflammation , microbiology and biotechnology , nf κb , signal transduction , copd , cadherin , chemistry , medicine , cancer research , biology , immunology , cell , biochemistry
Cigarette smoke exposure is a major cause of chronic obstructive pulmonary disease (COPD), but the underlying molecular inflammatory mechanisms remain poorly understood. Previous studies have found that smoke disrupts cell-cell adhesion by inducing epithelial barrier damage to the adherens junction proteins, primarily E-cadherin (E-cad) and p120-catenin (p120). Recently, the anti-inflammatory role of p120 has drawn increasing attention. In this study, we demonstrate that p120 has a role in the cigarette smoke extract-induced inflammatory response, presumably by regulating NF-κB signaling activation. Mechanistically, we show that p120-mediated NF-κB signaling activation in airway epithelial inflammation is partially RhoA dependent and is independent of E-cad. These results provide novel evidence for the role of p120 in the anti-inflammatory response.